Urinary biomarkers in hexachloro-1:3-butadiene-induced acute kidney injury in the female Hanover Wistar rat; correlation of α-glutathione S-transferase, albumin and kidney injury molecule-1 with histopathology and gene expression.
In contrast, the overall transcriptome (P < 0.001) and transcripts of preselected acute kidney injury (AKI) genes were significantly different between the groups, with kidney injury molecule 1 (P = 0.001) and neutrophil gelatinase-associated lipocalin (P = 0.002) being most highly expressed and genes associated with glutathione metabolism (GSTA1, 3 and 4) most down-regulated in kidneys with subsequent severe dysfunction.
Therefore, we comprehensively addressed the relationship between Ucr-correction and UFR-correction of ten urinary biomarkers N-acetyl-β-d-glucosaminidase (NAG), lactate dehydrogenase (LDH), total protein, albumin, kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, clusterin, β(2)-microglobulin, cystatin-c and glutathione S-transferase-α in non-steady state situations such as AKI.
We evaluated urine (u) sistatin-C (uCys-C), kidney injury molecule-1 (uKIM-1) and neutrophil gelatinase associate lipocaline (uNGAL) as markers of AKI.
In summary, we report noninvasive detection of AKI in humans by combining the sensitivity of KIM-1 along with mechanistic potentials of miR-21, -200c, and -423.
Urinary KIM-1 displayed the highest AUC of 0.81 (95% confidence interval [CI], 0.76-0.93; P < 0.001) for the early detection of AKI after circulatory collapse, followed by NGAL (0.77% CI, 0.70-0.84) and IL-18 (0.69% CI, 0.48-0.64).
After the description of the pathophysiology of "prerenal azotemia" and of Acute Kidney Injury (AKI) due to ischemia or nephrotoxicity, the renal biomarkers are listed and described: urinary NAG, urinary and serum KIM-1, serum and urinary NGAL, urinary IL-18, urinary L-FABP, serum Midkine, urinary IGFBP7 and TIMP2, urinary α-GST and π-GST, urinary ɣGT and AP, urinary β<sub>2</sub>M, urinary RBP, serum and urinary miRNA.
Plasma heart-type fatty acid-binding protein was higher 12 hours after reperfusion in AKI patients, though urinary kidney injury molecule 1 and neutrophil gelatinase-associated lipocalin were similar between those with or without AKI.
SP-D polymorphisms Thr11Met and Thr160Ala, AKI patient serum SP-D levels at days 1, 3 and 7 and urine KIM-1 levels in both AKI patients and controls were examined.
Both plasma and urinary KIM-1 expression levels were significantly higher in AKI and chronic kidney disease (CKD) patients than in healthy volunteers, and urinary KIM-1 expression was significantly higher in CKD patients than in AKI patients.
What is new: • Urinary calprotectin and KIM-1 do not predict mortality in our heterogeneous pediatric AKI cohort, but they show moderate performance in the prediction of dialysis.
Urinary NGAL significantly rise in AKI patients 2 and 6 hr after CPB with corresponding AUC of (0.710 and 0.700) but uKIM-1 was higher in the AKI group 12 and 24 hr after CPB with AUC (0.725 and 0.703) respectively.
In addition, serum NGAL values (404± 269 vs 116± 78 ng/mL, P<0.001), KIM-1 values (0.80± 0.52 vs 0.33± 0.68 ng/mL, P<0.001), urine NGAL/creatinine values (371± 672 vs 27± 39 ng/mg, P<0.001) and urine KIM-1/creatinine values (4.04± 2.43 vs 2.38± 1.89 ng/mg, P<0.001) were higher in the AKI group than in the non-AKI group.